Document Detail


Transient inactivation of basolateral amygdala during selective satiation disrupts reinforcer devaluation in rats.
MedLine Citation:
PMID:  22845705     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Basolateral amygdala (BLA) function is critical for flexible, goal-directed behavior, including performance on reinforcer devaluation tasks. Here we tested, in rats, the hypothesis that BLA is critical for conditioned reinforcer devaluation during the period when the primary reinforcer (food) is being devalued (by feeding it to satiety), but not thereafter for guiding behavioral choices. We used a spatially independent task that used two visual cues, each predicting one of two foods. An instrumental action (lever press) was required for reinforcer delivery. After training, rats received BLA or sham lesions, or cannulae implanted in BLA. Under control conditions (sham lesions, saline infusions), devaluation of one food significantly decreased responding to the cue associated with that food, when both cues were presented simultaneously during extinction. BLA lesions impaired this devaluation effect. Transient inactivation of BLA by microinfusion of the γ-aminobutyric acid receptor type A agonist muscimol resulted in an impairment only when BLA was inactivated during satiation. When muscimol was infused after satiation and therefore, BLA was inactivated only during the choice test, rats showed no impairment. Thus, BLA is necessary for registering or updating cues to reflect updated reinforcer values, but not for guiding choices once the value has been updated. Our results are the first to describe the contribution of rat BLA to specific components of reinforcer devaluation and are the first to show impairment in reinforcer devaluation following transient inactivation in the rat.
Authors:
Elizabeth A West; Patrick A Forcelli; Alice T Murnen; David L McCue; Karen Gale; Ludise Malkova
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Behavioral neuroscience     Volume:  126     ISSN:  1939-0084     ISO Abbreviation:  Behav. Neurosci.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-07-31     Completed Date:  2012-12-20     Revised Date:  2013-08-12    
Medline Journal Info:
Nlm Unique ID:  8302411     Medline TA:  Behav Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  563-74     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20007, USA.
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MeSH Terms
Descriptor/Qualifier:
Amygdala / drug effects,  injuries,  physiology*
Analysis of Variance
Animals
Choice Behavior / drug effects,  physiology*
Conditioning, Operant / drug effects,  physiology*
Cues
Excitatory Amino Acid Agonists / toxicity
Extinction, Psychological / drug effects,  physiology*
Food
Functional Laterality / drug effects,  physiology
GABA-A Receptor Agonists / pharmacology
Male
Muscimol / pharmacology
N-Methylaspartate / toxicity
Rats
Rats, Long-Evans
Reinforcement (Psychology)*
Grant Support
ID/Acronym/Agency:
F31 DA026705/DA/NIDA NIH HHS; F31DA026705/DA/NIDA NIH HHS; F31NS066822/NS/NINDS NIH HHS; T32DA007291/DA/NIDA NIH HHS; T32NS04123/NS/NINDS NIH HHS; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/Excitatory Amino Acid Agonists; 0/GABA-A Receptor Agonists; 2763-96-4/Muscimol; 6384-92-5/N-Methylaspartate
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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